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MEDLINE
1999397656 MEDLINE
99397656 PubMed ID: 10471055

Analysis of potential markers for detection of
submicroscopic lymph node metastases in breast
cancer .

Merrie A E; Yun K; Gunn J; Phillips L V; McCall J L

Department of Surgery, Dunedin School of Medicine,

University of Otago, New Zealand.

BRITISH JOURNAL OF CANCER, (1999 Aug) 80 (12)

2019-24.

Journal code: 0370635. ISSN: 0007-0920.

SCOTLAND: United Kingdom

Journal; Article; (JOURNAL ARTICLE)

English

Priority Journals
199909

Entered STN: 19991005

Last Updated on STN: 20000303

Entered Medline: 19990921

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AB We have developed sensitive assays for- cytokeratin (K) 8, 16, 19,
stromelysin 3 (ST3), MUC1 and maspin mRNAs using reverse

transcription polymerase chain reaction (RT-PCR) and used these to assess
lymph node status in patients undergoing surgery for breast cancer. In
addition the RT-PCR assays were tested against lymph nodes from
non-cancer

patients to determine their specificity. Despite high sensitivity RT-PCR
assays for K8, K16, K19, ST3 and maspin were not found to be
useful as markers of submicroscopic disease as transcripts of these genes
were detected in the great majority of control lymph nodes tested.
Expression of MUC1 was also not found to be useful as it was both
insensitive and non-specific. The importance of assessing potential
markers against an adequately sized control population is demonstrated,

failure to do so can lead to erroneous conclusions.

LI 8 ANSWER 7 OF 24 MEDLINE

ACCESSION NUMBER: 1998031853 MEDLINE

DOCUMENT NUMBER: 98031853 PubMed ID: 9366525

TITLE: Evidence of a dominant transcriptional pathway which

regulates an undifferentiated and complete
metastatic phenotype.
AUTHOR: Barsky S H; Sternlicht M D; Safarians S; Nguyen M; Chin K;

Stewart S D; Hiti A L; Gray J W
CORPORATE SOURCE: Department of Pathology, University of California Los

Angeles School of Medicine 90024, USA.
CONTRACT NUMBER: CA01351 (NCI)

CA40225 (NCI)
CA56735 (NCI)
+

SOURCE: ONCOGENE, (1997 Oct 23) 15 (17) 2077-91.

Journal code: 8711562. ISSN: 0950-9232.
PUB. COUNTRY: ENGLAND : United Kingdom

DOCUMENT TYPE: Journal; Article; (JOURNAL ARTICLE)

LANGUAGE: English
FILE SEGMENT: Priority Journals

ENTRY MONTH: 199711

ENTRY DATE: Entered STN: 19971224

Last Updated on STN: 19971224
Entered Medline: 19971120
AB The highly metastatic amelanotic C8161 human melanoma line was found to
exhibit complete dominance of its undifferentiated and metastatic
phenotype in multiple somatic cell hybridization studies designed to
bypass the presence of potential tumor suppressor genes. In a three

armed

approach involving somatic cell fusions of C8161 with recipient lines of
greater differentiation, different lineage, and different tumorigenicity
status, the metastatic and undifferentiated phenotype of C8161 was
promiscuously dominant. In somatic cell hybrids produced between the
C8161 and a group of non-metas tatic human melanoma lines which exhibited
melanocyte differentiation markers including S100, HMB-45, NKI/C3, and
melanin, the fusions were uniformly metastatic and undifferentiated. In
somatic cell hybrids of C8161 and MCF-7 the fusions exhibited an estrogen
independent and unresponsive, estrogen receptor (ER) negative, and highly
metastatic phenotype. In fusions between C8161 and HMS-1, an
immortalized

'benign 1 human myoepithelial line which produced an abundant
extracellular

matrix (ECM) and high levels of protease and angiogenic inhibitors
including maspin, tissue inhibitor of metalloproteinase-1
(TIMP-1), alphal-antitrypsin ( alpha 1-AT ) , protease nexin II (PN-II),
thrombospondin-1 and soluble basic fibroblast growth factor (bFGF)
receptors, the hybrids showed complete absence of matrix, absent
maspin expression, markedly decreased protease inhibitor and
angiogenic inhibitor production, high levels of proteases and angiogenic
factors, and a highly metastatic phenotype. In our somatic cell fusions,
the human-human hybrids represented true and complete fusions and not
hybrid clones selected for by loss of dominant-acting growth suppressor
genes. This finding was supported by detailed comparative genomic
hybridization (CGH) studies, Q-banding karyotype analysis, and
autofusions

of representative clones. The purposeful creation of inherently unstable
human-murine fusions between C8161 and B16-F1 where loss of putative

suppressor loci would be expected, resulted in fusions exhibiting
decreased growth and non-metastatic behavior with progressive chromosomal
loss. Neither p53, nm23, DNA methyltransf erase, activated ras,
fibroblast

growth factor-4 (FGF-4), or epidermal growth factor receptor (EGFR)
mediated the acquisition of the metastatic or undifferentiated phenotype
within the C8161-human fusions. These studies are the first studies ever
to successfully transfer the complete metastatic phenotype by somatic

cell

fusion and support the presence of a new high level regulatory pathway (s)
involving dominant trans-acting factors which act pleiotropically to
regulate an undifferentiated and highly metastatic phenotype.

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MEDLINE
97218145 MEDLINE
97218145 PubMed ID:
Rat and human maspins
metastatic suppressor
prostate cancer cells.
Umekita Y; Hiipakka R A; Liao S
The Ben May Institute

9065806

structures,
activity and mutation in

but

for Cancer Research , Department of
Biochemistry and Molecular Biology, University of Chicago,
IL 60637, USA.
CA58073 (NCI)

CANCER LETTERS, (1997 Feb 26) 113 (1-2) 87-93.
Journal code: 7600053. ISSN: 0304-3835.
Ireland

Journal; Article; (JOURNAL ARTICLE)
English

Priority Journals
GENBANK-U5 8857
199704

Entered STN: 19970422
Last Updated on STN: 19970422
Entered Medline: 19970407
The rat homologue of human maspin cDNA was cloned. The deduced
amino acid sequence of rat maspin was homologous to human
maspin with 88% of the amino acids conserved. Rat maspin
mRNA was detected in rat mammary gland, vagina, urinary bladder, thymus,
small intestine, skin, ventral prostate, seminal vesicles, and thyroid

not in many other organs, such as heart, lung, liver, brain and kidney.
Rat maspin cDNA retrovirally introduced into highly metastatic
Dunning AT3 . 1 rat prostate cancer cells did not suppress metastasis of
these tumor cells in Copenhagen rats. Maspin mRNA was detected
in 5/10 human prostatic carcinoma tissue samples. Two human prostate
cancer cell lines, PC-3 and LNCaP, and two human prostatic carcinoma and
two benign prostatic hyperplasia tissue samples contained maspin
mRNA having an isoleucine to valine mutation at amino acid 319.

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297B.

American

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Research

April

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24 BIOSIS COPYRIGHT 2003 BIOLOGICAL ABSTRACTS INC.
1997:56907 BIOSIS
PREV199799356110

Expression of maspin by human breast tumor cells
inhibits primary tumor cell growth and lung
metastasis in an athymic mouse model.

Ding, I.; Huang, H. D.; Sabet, H.; Zou, Z. Q. ; Zhang, L.
R.; Kern, F. G. ; Okunieff, P.

Radiation Oncol. Branch, NCI, NIH, Bethesda, MD USA
Blood, (1996) Vol. 88, No. 10 SUPPL. 1 PART 1-2, pp.

Meeting Info.: Thirty-eighth Annual Meeting of the

Society of Hematology Orlando, Florida, USA December 6-10,
1996

ISSN: 0006-4971.
Conference; Abstract
English

24 BIOSIS COPYRIGHT 2003 BIOLOGICAL ABSTRACTS INC.
1996:254732 BIOSIS
PREV199698810861

Differential expression of Maspin protein in
human adenocarcinomas and squamous cell
carcinomas .

Ding, I.; Zou, Z. Q. ; Huang, H. D.; Zhang, K. ; Zhang, L.
R.; Tang, D.; Okunieff, P.

Natl. Cancer Inst., NIH, Bethesda, MD 20892 USA
Proceedings of the American Association for Cancer

Annual Meeting, (1996) Vol. 37, No. 0, pp. 90.
Meeting Info.: 87th Annual Meeting of the American
Association for Cancer Research Washington, D.C., USA

20-24, 1996
ISSN: 0197-016X.
Conference
English

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SCISEARCH COPYRIGHT 2003 THOMSON ISI
1998 : 80377 SCISEARCH
BK17U

Maspin - A tumor suppressing serpin (Reprinted
from Attempts to Understand Metastasis Formation
I: Metastasis-Related Molecules, 1996)

Sager R (Reprint) ; Sheng S; Pemberton P; Hendrix M J C
DANA FARBER CANC INST, DIV CANC GENET, 44 BINNEY ST,
BOSTON, MA 02115 (Reprint)
USA

ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY, (JAN
1997) Vol. 425, pp. 77-88.

Publisher: PLENUM PRESS DIV PLENUM PUBLISHING CORP, 233

SPRING ST, NEW YORK, NY 10013.

ISSN: 0065-2598.

Reprint; Journal

English

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SCISEARCH COPYRIGHT 2003 THOMSON ISI
97 : 190621 SCISEARCH
WK895

The role of serpin superfamily members in cancer
Pemberton P A (Reprint)

LXR BIOTECHNOL, 14 01 MARINA WAY S, RICHMOND, CA 94 8 04
(Reprint)
USA

CANCER JOURNAL, (JAN- FEB 1997) Vol. 10, No. 1,
pp. 24-30.

Publisher: ASSOC DEVELOPPEMENT COMMUNICATION
CANCEROLOGIQUE, CANCER JOURNAL, 7 RUE GUY MOQUET, BP 8,
94801 VILLEJUIF, FRANCE.
ISSN: 0765-7846.
General Review; Journal
LIFE
English
48

^ABSTRACT IS AVAILABLE IN THE ALL AND I ALL FORMATS*
The f 'serpin'' class of serine proteinase inhibitors was originally
shown to be involved in suppression of tumor invasion by their direct
inhibitory actions on the matrix-degrading serine proteinases uPA and
plasmin, It is now clear that individual members play a variety of roles
in tumorigenesis, from regulating differentiation events, to inhibiting
cysteine proteinases involved in matrix degradation and selection
processes associated with tumor survival (apoptosis), Not all of these
roles involve proteinase inhibition mediated by the serpin reactive site
loop (RSL) , instead other domains have been identified that confer these
activities, and in some cases the RSL itself appears to have lost
inhibitory activity and evolved a ligand-binding function, Several
serpins

involved in these processes map to the same locus on chromosome 18q21.3 (
maspin, SCCA1, SCCA2, PAI-2), indicating that they arose by
duplication of a common ancestral gene, It appears that these serpins and
their target proteinases and/or ligands have evolved to control cellular
proliferation and migration events and should therefore be examined more
closely during tumor progression, and considered as key targets for the
development of novel therapeutic anti-cancer agents.

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96653574
96653574

Differential expression of maspin protein in
human adenocarcinomas and squamous cell
carcinomas (Meeting abstract) .

Ding I; Zou Z Q; Huang K D; Zhang K; Zhang L R; Tang D;
Okunieff P

National Cancer Institute, Bethesda, MD 20892.
Proc Annu Meet Am Assoc Cancer Res, (1996) 37
A627.

ISSN: 0197-016X.
(MEETING ABSTRACTS)
English

Institute for Cell and Developmental Biology
199609

Entered STN: 19970509
Last Updated on STN: 19970509
Using the differential display method, Maspin/ a member of the
Serpin family of proteinase inhibitors, has been identified by screening
the mRNA expression of normal human breast epithelium and tumor cells.
Normal mammary epithelial cells, but not tumor cells or breast-derived
fibroblasts, express Maspin- This distribution is consistent
with the proposed tumor suppression associated with Maspin
protein. In order to determine if the Maspin protein expression
is important in carcinogenesis at other sites, 10 adenocarcinoma and 11
squamous cell carcinomas cell lines were tested for the
Maspin protein expression by Western analysis. Adenocarcinoma cell
lines included 7 ovarian and three endometrial tumor lines, and
squamous cell tumors included 8 cervical carcinoma and 3 oral or
skin carcinoma lines. None of the ovarian tumor lines (0/7) and only one
of three of endometrial tumor lines had even moderate Maspin
protein expression. However, seven of eight cervical carcinoma cell lines
and two of three squamous cell carcinoma cell lines (SCC4 and
A431) highly expressed the Maspin protein. Immunohistochemistry
was done on tumor specimens from 27 ovarian and 9 esophageal carcinomas.
44% (12/27) of ovarian tumors and 77% (7/9) esophageal carcinoma
specimens

had either focal or diffuses Maspin immunoreactivity determined

by an immunohis tochemical staining using a polyclonal antibody. Our

results indicate that the expression of Maspin plays a role in

several human tumors, including ovary, cervix, endometrium, esophagus and

tongue. The Maspin protein expression was less common in

adenocarcinomas but was commonly overexpressed in squamous cell

carcinomas.

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CAPLUS COPYRIGHT 2003 ACS
1999:654663 CAPLUS
132:120643

New genes potentially involved in breast cancer
metastasis

Schwirzke, Marina; Schiemann, Sabine; Gnirke, Andrea
U. ; Weidle, Ulrich H.

Roche Pharmaceuticals, Penzberg, D-82372, Germany
Anticancer Research (1999), 19 (3A) ,
1801-1814

CODEN: ANTRD4; ISSN: 0250-7005

International Institute of Anticancer Research
Journal; General Review
English

A review, with 135 refs. Identification of new genes involved in the
pathogenesis of breast cancer opens new avenues for improved diagnostic
markers and new mol . targets for improved treatment of this malignancy.
In the following we review genes with proved involvement in invasion and
metastasis of breast cancer as well as genes which exhibit an expression
pattern that correlates with invasion and metastasis.
REFERENCE COUNT: 135 THERE ARE 135 CITED REFERENCES AVAILABLE FOR

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AB

L18 ANSWER 24 OF 24 CAPLUS COPYRIGHT 2003 ACS
ACCESSION NUMBER: 1998:671816 CAPLUS

DOCUMENT NUMBER: 130:33609

TITLE: Identification of superior markers for polymerase

chain reaction detection of breast cancer
metastases in sentinel lymph nodes

AUTHOR (S) : Min, C. Justus; Tafra, Lorraine; Verbanac, Kathryn M.

CORPORATE SOURCE: Departments of Biology, East Carolina University,

Greenville, NC, 27858, USA

SOURCE: Cancer Research (1998), 58(20), 4581-4584

CODEN: CNREA8; ISSN: 0008-5472

PUBLISHER: American Association for Cancer Research

DOCUMENT TYPE: Journal

LANGUAGE: English

AB Sentinel lymph node biopsy (SLNB) is being evaluated in breast cancer
patients to improve detection of metastases and to guide therapy with
minimal morbidity. The use of reverse transcription-PCR anal, to

increase

detection of tumor cells in SLN of breast cancer patients is hampered by
the lack of specific markers. In this study, seven markers were
evaluated

by reverse transcription-PCR for expression in human breast
adenocarcinoma

lines (BrCa) and in normal nodes from non-cancer patients. Two markers
yielded exceptional results; mammaglobin and carcinoembryonic antigen
transcripts were detected in 100 and 71% BrCa, resp., and were absent

from

all normal lymph nodes . These markers will be used as components of a
multimarker panel to evaluate sentinel nodes in an on-going, multicenter
clin. trial.

REFERENCE COUNT: 2 0 THERE ARE 20 CITED REFERENCES AVAILABLE FOR

THIS

RECORD. ALL CITATIONS AVAILABLE IN THE RE

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L15 ANSWER 50 OF 64

MEDLINE

ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

90024082 MEDLINE
90024082 PubMed ID: 2802033

Prognostic factors in squamous cell carcinoma of
the larynx.

Eiband J D; Elias E G; Suter C M; Gray W C; Didolkar M S
Department of Surgery, University of Maryland, Baltimore.
AMERICAN JOURNAL OF SURGERY, (1989 Oct) 158 (A)
314-7.

Journal code: 0370473. ISSN: 0002-9610.
United States

Journal; Article; (JOURNAL ARTICLE)
English

Abridged Index Medicus Journals; Priority Journals
198910

Entered STN: 19900328
Last Updated on STN: 19900328
Entered Medline: 19891031
One hundred fifty-two patients with squamous cell carcinoma of
the larynx were studied. The disease-free survival and overall survival
rates were correlated to 12 variables. Seven of them seemed to affect
survival. Poor prognosis was related to (1) advanced stage of disease at
diagnosis, (2) cord fixation and massive local invasion, (3) ulceration

AUTHOR:

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the primary tumor, (4) lymph node metastases

at diagnosis, (5) glottic lesions had a poorer prognosis than
supraglottic

ones, (6) locoregional recurrences, and (7) male gender. However, most of
these significant differences were in disease-free survival, and
only primary tumor staging; lymph

node status; and locoregional recurrences affected overall
survival. On the other hand, the other five variables showed no effect on
either disease-free or overall survival rates. These included age, race,
cell differentiation, type of recurrence, and the initial definitive
therapeutic modality.

L15 ANSWER 52 OF 64 MEDLINE
ACCESSION NUMBER: 88159836 MEDLINE
DOCUMENT NUMBER: 88159836 PubMed ID: 2450417

TITLE : Is there a place for liver grafting for malignancy?.

AUTHOR: Pichlmayr R

CORPORATE SOURCE: Klinik fur Abdominal -und Transplantationschirurgie,

Medizinische Hochschule, Hannover, FRG.
SOURCE: TRANSPLANTATION PROCEEDINGS, (1988 Feb) 20 (1

Suppl 1) 478-82.

Journal code: 0243532. ISSN: 0041-1345.
PUB . COUNTRY: United States

DOCUMENT TYPE: Journal; Article; (JOURNAL ARTICLE)

LANGUAGE: English

FILE SEGMENT: Priority Journals

ENTRY MONTH: 198804

ENTRY DATE: Entered STN: 19900308

Last Updated on STN: 19900308
Entered Medline: 19880411

AB In 94 patients liver transplantations for malignant tumors of the liver
have been performed in this institution from 1972 to 1987. The long-term
overall results in hepatic transplantation for irresectable tumors are
disappointing in spite of good short-term palliation in most of the
patients. Tumor recurrence is the rule. But individual long-living
patients demonstrate the potentials of this treatment. Thus the crucial
question will be a proper selection of patients. The relative suitability
(in descending order of f avorableness ) of the kinds of tumors may range
from HCC without cirrhosis, to central bile duct tumors, to HCC in
cirrhosis, to CCC, and finally to secondaries. But this range can only
give some probability for the success rate. More important is the
tumor stage- Survival in lymph

node-positive stages is by far worse than in lymph

node-negative stages. The 6-month, 1-year, and 2-year actuarial

survival data in our experience for lymph node

-negative (lymph node-positive) HCC without cirrhosis

are 83%, 75%, 75% (33%, 11%, 11%); in bile duct carcinomas in

lymph node-negative stages (lymph node

-positive) they are 6 months, 100% (40%); 1 year, 100% (13%); and 2
years,

83% (0%). Hepatic transplantation for selected tumor patients furthermore
seems justified and is essential for a detailed analysis of the chance of
different tumor types for success with this method of treatment.

L15 ANSWER 53 OF 64 MEDLINE

L15 ANSWER 53 OF 64 MEDLINE
ACCESSION NUMBER: 88251178 MEDLINE
DOCUMENT NUMBER: 88251178 PubMed ID: 3289517

TITLE: Surgical management of lung cancer with solitary cerebral

metastasis .

AUTHOR ; Hankins J R; Miller J E; Salcman M; Ferraro F; Green D C;

Attar S; McLaughlin J S
CORPORATE SOURCE: Department of Surgery, University of Maryland School of

Medicine, Baltimore.
SOURCE: ANNALS OF THORACIC SURGERY, (1988 Jul) 4 6 (1)

24-8. Ref: 20

Journal code: 15030100R. ISSN: 0003-4975.
PUB. COUNTRY: United States

DOCUMENT TYPE: Journal; Article; (JOURNAL ARTICLE)

General Review; (REVIEW)

(REVIEW, TUTORIAL)
LANGUAGE: English

FILE SEGMENT: Abridged Index Medicus Journals; Priority Journals

ENTRY MONTH: 198807

ENTRY DATE: Entered STN: 19900308

Last Updated on STN: 19900308
Entered Medline: 19880726

AB Between 1964 and 1986, 19 patients underwent resection of both a primary
lung cancer and the associated brain metastasis- One patient
underwent resection of 2 separate primary lung cancers and the associated
metastases. The 12 men and 7 women ranged in age from 42 to 67
years (mean, 54.6 years). The cell type was adenocarcinoma in 12 tumors,
squamous or adenosquamous cell in 5, large cell undifferentiated or
anaplastic in 2, and malignant carcinoid in 1 tumor. The types of
resection were as follows: lobectomy for 12 neoplasms, pneumonectomy for
5, bilobectomy for 2, and wedge resection for 1 neoplasm. Radiotherapy to
the brain was given in connection with sixteen of the twenty

craniotomies -

The patient with 2 separate primary neoplasms survived 19 years before
dying 5 months after the second craniotomy. The mean survival is 8.0 +/-
2.1 years {+/- the standard error), and the median survival is 1.67
years .

Survival at 1 year was 65 +/- 10.7% and at 5 years, 45 +/- 11.1%. On
univariate analysis, the following factors were found to correlate
significantly with longer survival: a lung tumor in
Stage I or II; negative mediastinal nodes; curative rather than
palliative resection of the lung tumor; and age younger than 55 years.
However, on multivariate analysis, only curative resection was a
significant factor (p less than 0.01). We believe these results justify
continued application of this combined surgical approach to patients
having limited-stage lung cancer with a solitary brain metastasis

LIS ANSWER 54 OF 64 MEDLINE

ACCESSION NUMBER: 89015968 MEDLINE

DOCUMENT NUMBER: 89015968 PubMed ID: 3140177

TITLE: Squamous cell carcinoma of the soft palate,

uvula, and anterior faucial pillar.
AUTHOR: Weber R S; Peters L J; Wolf P; Guillamondegui 0

CORPORATE SOURCE: Department of Head and Neck Surgery, University of Texas

M.D. Anderson Hospital and Tumor Institute, Houston

77030.

SOURCE: OTOLARYNGOLOGY - HEAD AND NECK SURGERY, (1988 Jul)

99 (1) 16-23.

Journal code: 8508176. ISSN: 0194-5998.
PUB. COUNTRY: United States

DOCUMENT TYPE: Journal; Article; (JOURNAL ARTICLE)

LANGUAGE: English

FILE SEGMENT: Priority Journals

ENTRY MONTH: 198810

ENTRY DATE: Entered STN: 19900308

Last Updated on STN: 19900308
Entered Medline: 19881031

AB This retrospective study concerns 188 patients with squamous cell
carcinoma of the soft palate, uvula, and anterior faucial pillar
treated for cure between 1970 and 1983. Men predominated in the group
(1.9:1) and 55% of the patients were between 60 and 70 years old. Mean
duration of followup was 56.7 months. TNM stage distribution was 29, 67,
37, and 49 patients for stages I, II, III, and IV respectively; six
patients were unstaged because of previous excisional biopsy. Treatment

alone
for

the primary site consisted of radiotherapy for 150 patients, surgery

for 28 patients, and combined therapy for 10 patients. Primary control

T stages 1 through 4 was: 91% (31 of 34), 77% (71 of 92), 77% (30 of 39),
and 35% (6 of 17), respectively. One hundred twenty-eight patients were

at presentation, as compared to 60 patients with regional nodal

metastasis- Regional control was obtained in 87.5% of patients

with NO necks and in 76.7% of those with nodal involvement. In patients

with primary control, these figures were 89% and 81%. Overall determinant

survival was 80% at 2 years, but fell to 67% at 5 years. In addition to

advanced tumor stage, the survival rate was

reduced by regional lymph node metastasis*

Tumor extension to the tongue base diminished survival. Survival was
poorer among patients with midline tumors or tumors that extended across
the palatine arch (37 patients) than for those with unilateral primary
tumors (151 patients) (p less than 0.05). Despite similar T-stage
distribution, the incidence of regional nodal metastasis was 49%
in the former group, compared with 28% in the latter. (ABSTRACT TRUNCATED
AT 250 WORDS)

LIS ANSWER 55 OF 64 BIOSIS COPYRIGHT 2002 BIOLOGICAL ABSTRACTS INC.
ACCESSION NUMBER: 1988:73232 BIOSIS
DOCUMENT NUMBER: BA85: 39531

TITLE : CARCINOMA OF THE COLON LONG-TERM SURVIVAL AND

PROGNOSIS AFTER SURGICAL TREATMENT IN A SERIES OF 798
PATIENTS.

AUTHOR (S): MOREAUX J; CATALA M

CORPORATE SOURCE: CENT. MEDICO- CHI RURGICAL DE LA PORTE DE CHOISY, 15 AVENUE

DE LA PORTE DE CHOISY, 75013 PARIS, FR.

SOURCE: WORLD J SURG, (1987) 11 (6), 804-808.

CODEN: WJSUDI. ISSN: 0364-2313.

FILE SEGMENT: BA; OLD

LANGUAGE: English

AB From 1964 to 1985, a total of 798 patients (405 female, 393 male) were

operated on for a single cancer of the colon. Fifty-eight percent of the
patients were between 60 and 80 years of age. Liver and/or peritoneal
metastases were present in 16.3% of the 818 cases. Resection was
performed in 754 cases (92.2%), and was considered to be curative in 646
(78.9%). Tumors were differentiated in 90.5% of the cases. Regional
lymph nodes were involved in 33.3% and serosal

penetration was present in 19.5% of the cases. There were 7 postoperative
deaths, 3 (0.5%) of them after curative resection. The actuarial curves

survival showed a probability of survival after all operations of 62% at

years and 46% at 10 years, and after curative resection of 78% at 5 years
and 58% at 10 years. Prognosis has been established from the 513 patients
operated on before 1980; follow-up data were available for all but 4 of
them. Tumor site in the right or left colon did not relate significantly
to survival. Tumor staging was the main

prognostic factor. The 5-year survival rate was 40% in patients with
positive nodes, 74.7% in those with negative nodes (p < 0.001), 97.6% in
those with invasion limited to mucosa or submucosa, and 41.9% in those
with serosal invasion (p < 0.001). Based on Dukes' classification, the
5-year survival rates for A, B, C, and D tumors were 91%, 76.7% (p =
0.01), 53.1% (p < 0.001), and 4.7% (p < 0.001), respectively. Time
elapsed

between first symptom and operation did not relate significantly to
survival. Prognosis was better in patients less than 50 years old when
compared with patients 50-70 years of age (p < 0.01), and was better in
female patients than in male patients (p = 0.02).

LIS ANSWER 49 OF 64 MEDLINE DUPLICATE 23

ACCESSION NUMBER: 90068906 MEDLINE
DOCUMENT NUMBER: 90068906 PubMed ID: 2587716
TITLE: [Percutaneous radiotherapy for thyroid gland

carcinoma] •

Ergebnisse der perkutanen Strahlentherapie bei
Schilddrusenkarzinomen.
AUTHOR: Kleinert G

SOURCE: RADIOBIOLOGIA, RADIOTHERAPIA, (1989) 30 (5)

473-80.

Journal code: 0401247. ISSN: 0033-8184.
PUB. COUNTRY: GERMANY, EAST: German Democratic Republic

DOCUMENT TYPE: Journal; Article; (JOURNAL ARTICLE)

LANGUAGE: German
FILE SEGMENT: Priority Journals

ENTRY MONTH: 199001

ENTRY DATE: Entered STN: 19900328

Last Updated on STN: 19900328
Entered Medline: 19900110

AB Prognostically relevant factors as well as indications for percutaneous
radiotherapy are analysed by the hand of a retrospective analysis of
therapeutic results in 86 patients that were exposed a percutaneous
radiotherapy because of a thyroid carcinoma at the Clinic and
Policlinic of the Medical Academy Erfurt during the period 1972 to 1982.
The 5-years-survivals of 83% for patients with differentiated
carcinoma and 22% for patients with dedifferentiated
carcinoma prove the influence of tumor histology on prognosis of
the disease. Next to it the locoregional tumor spreading at beginning of
therapy rendered prognostically relevant. The 5-years-survival
was 83% in tumor stages T1-3N0M0. With
metastatic infiltration into lymph-nodes of

the neck the 5-years-survival decreased to 57%, with spreading of the
primary tumor beyond organ borders to 23,5%. The postoperative
percutaneous radiotherapy should be applied in all cases of
metastatic infiltration of lymph-nodes- In

large, inoperable tumors the percutaneous radiotherapy is the solely
possible palliative measure that should be applied both in differentiated
and also in anaplastic carcinomas in spite of infaust prognosis.

LIS ANSWER 59 OF 64
ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

MEDLINE
85095913 MEDLINE
85095913 PubMed ID: 2981516

Surgical therapeutic planning for non-small cell lung
cancer .

Sawamura K; Mori T; Hashimoto S; Iuchi K; Tada H; Lee Y E;
Mizuta T; Ichimiya A; Akashi A

GAN TO KAGAKU RYOHO [JAPANESE JOURNAL OF CANCER AND
CHEMOTHERAPY] , (1985 Jan) 12 (1) 36-44.
Journal code: 7810034, ISSN: 0385-0684.
Japan

Journal; Article; (JOURNAL ARTICLE)
Japanese

Priority Journals
198502

Entered STN: 19900320

Last Updated on STN: 19900320

Entered Medline: 19850214

AUTHOR:

SOURCE :

PUB . COUNTRY:
DOCUMENT TYPE:
LANGUAGE :

FILE SEGMENT:
ENTRY MONTH:
ENTRY DATE:

AB The survival rates of 380 resected cases of lung cancer in our hospital
were analyzed according to curability and histological cell type. The
overall 5-year survival rate for stage I a cases was 64.5%, that for

stage

I b 52.3%, and that for stage II 26.7%. However, there were distinct
differences in survival rates between stages I a-II with mediastinal
lymph node dissection and those without mediastinal
lymph node dissection. Of these 380 tumors, many were

advanced (for instance, stage III tumors comprised 180 cases). T3 tumors
had better prognosis (40.7% showing 5-year survival) than N2 tumors
(26.7%

showing 5-year survival) - Among stage III

tumors, squamous cell carcinoma (T3: 41%, N2 : 36.7%

showing 5-year survival) had a better prognosis than adenocarcinoma (T3:
16.1%, N2: 21.4%). T3N2 tumors, however, had such a poor prognosis that
the value of surgery in these cases seemed questionable. Adjuvant therapy
should therefore be evaluated accurately in future to improve prognosis.
It was stressed that a randomized controlled study would be needed to
evaluate the effectiveness of adjuvant therapy.

AUTHOR:

LIS ANSWER 61 OF 64
ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

FILE SEGMENT:
ENTRY MONTH:
ENTRY DATE:

PUB. COUNTRY:
DOCUMENT TYPE:
LANGUAGE :

SOURCE:

; MEDLINE DUPLICATE 24

82276071 MEDLINE
82276071 PubMed ID: 6810406

Advanced carcinoma of the nasopharynx. A clinical
study of 274 patients.

Petrovich Z; Cox J D; Roswit B; MacKintosh R; Middleton R;
Ohanian M; Rao Y; Byhardt R W; Paig C; del Regato J A
RADIOLOGY, (1982 Sep) 144 (4) 905-8.
Journal code: 0401260. ISSN: 0033-8419.
United States

Journal; Article; (JOURNAL ARTICLE)
English

Abridged Index Medicus Journals; Priority Journals
198210

Entered STN: 19900317

Last Updated on STN: 19900317

Entered Medline: 19821012
AB A total of 274 patients with a diagnosis of nasopharyngeal

carcinoma was treated in eight Veterans Administration Hospitals
over a period of 22 years. Of the 274 patients, 256 (93%) had
squamous-cell carcinoma, while 18 (7%) had other tumors. Most of
the squamous-cell carcinoma patients (82%) had Stage IV disease;
cervical lymph node metastases were found in

193 (75%), and distant metastases were present in 22 (9%). The
actuarial 5-, 10-, and 15-year survival rates for the 256 squamous-cell
carcinoma patients were 15%, 10%, and 7%, while they were 4 9%,
42%, and 35% for the 18 patients with other tumors (p = 0.006). There was
a progressive decrease in 5-year survival with the increase in the
stage of tumor- The survival of the 63

patients without metastases was better than the survival of the

193 patients with cervical metastases (24% vs. 12% at 5 years, p

= 0.03). The presence of T4 disease or Initial Performance Status of less

than 80 on the Karnofsky Scale indicated a poor prognosis (p = 0.0001).

Treatment failure occurred in 83% of the patients by 2 years after

therapy

and was due to the lack of tumor control at the primary site. Advanced
(N3) cervical lymph node metastases

indicated that systemic tumor dissemination of the nasopharynx is an
uncommon malignancy.

L4 ANSWER 2 OF
ACCESSION NUMBER
DOCUMENT NUMBER:
TITLE :

AUTHOR (S) :

CORPORATE SOURCE
USA

SOURCE :
Research

Calif ornia,

DOCUMENT TYPE:

LANGUAGE :

6 BIOSIS COPYRIGHT 2001 BIOSIS
2000:270286 BIOSIS
PREV200000270286

High tumor maspin expression is associated with
improved survival of patients with oral
squamous cell carcinoma.

Xia, Weiya (1); Lau, Y.-K. (1); Hu, M. C.-T. (1); Li, L.
(1); Johnston, D. A. (1); Sheng, S.-J. (1); El-Naggar, A.
K. (1); Hung, M. C. (1)

(1) M D Anderson Cancer Ctr, Univ of Texas, Houston, TX

Proceedings of the American Association for Cancer

Annual Meeting, (March, 2000) No. 41, pp. 689. print..
Meeting Info.: 91st Annual Meeting of the American
Association for Cancer Research. San Francisco,

USA April 01-05, 2000
ISSN: 0197-016X.
Conference
English

L4 ANSWER 4 OF 6
ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

DUPLICATE 3

and

MEDLINE
1999458661 MEDLINE
99458661 PubMed ID: 10527881

Identification and cDNA cloning of headpin, a novel
differentially expressed serpin that maps to chromosome
18q.

Spring P; Nakashima T; Frederick M; Henderson Y; dayman G
Department of Head and Neck Surgery, M. D. Anderson Cancer
Center, Houston, Texas, 77030, USA.
1P50DE11906-01 (NIDCR)
CA16672 (NCI)
R2 9DE11689-01A1 (NIDCR)

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, (1999
Oct 14) 264 (1) 299-304.

Journal code: 9Y8; 0372516. ISSN: 0006-291X.
United States

Journal; Article; (JOURNAL ARTICLE)
English

Priority Journals
GENBANK-AF 169949
199911

Entered STN: 20000111
Last Updated on STN: 20000111
Entered Medline: 19991112
Differential display was used to identify a novel serpin (headpin)
underexpressed in squamous cell cancers of the oral

cavity. Headpin cDNA encoding a complete open reading frame was cloned

sequenced. Headpin is expressed in normal oral mucosal tissue,
skin, and cultured keratinocytes . Using Northern analysis and relative
reverse-transcription polymerase chain reaction (relative RT-PCR) ,
downregulation of headpin mRNA expression was demonstrated in oral
cavity squamous carcinomas. Northern blot analysis identified a
3. 3-kb headpin mRNA transcript. Headpin is a 391-amino-acid protein with
a theoretical molecular weight of 44 kDa. Hinge region homology at the
reactive site loop suggests that headpin belongs to the inhibitory class
of serine protease inhibitors. Headpin was mapped to 18q21 . 3/18q22 . This
region includes the ovalbumin serpins (ov-serpins) maspin,
SCCA1, SCCA2, and PAI-2. Furthermore,
frequent loss of heterozygosity (LOH)
cancer and other malignancies.
Copyright 1999 Academic Press.

AUTHOR :

CORPORATE SOURCE
CONTRACT NUMBER:

SOURCE

PUB . COUNTRY :

LANGUAGE :
FILE SEGMENT:
OTHER SOURCE:
ENTRY MONTH:
ENTRY DATE:

18q is recognized as a region for
in head and neck

L4 ANSWER 6 OF 6 CANCERLIT
ACCESSION NUMBER: 96653574 CANCERLIT
DOCUMENT NUMBER: 96653574

TITLE: Differential expression of maspin protein in

human adenocarcinomas and squamous cell carcinomas

(Meeting

abstract) .

AUTHOR: Ding I; Zou Z Q; Huang K D; Zhang K; Zhang L R; Tang D;

Okunieff P

CORPORATE SOURCE: National Cancer Institute, Bethesda, MD 20892.
SOURCE : Proc Annu Meet Am Assoc Cancer Res, (1996). Vol. 37, pp.

A627.

ISSN: 0197-016X.
DOCUMENT TYPE: (MEETING ABSTRACTS)

FILE SEGMENT: ICDB
LANGUAGE: English
ENTRY MONTH: 199609

AB Using the differential display method, Maspin, a member of the

Serpin family of proteinase inhibitors, has been identified by screening
the mRNA expression of normal human breast epithelium and tumor cells.
Normal mammary epithelial cells, but not tumor cells or breast-derived
fibroblasts, express Maspin. This distribution is consistent
with the proposed tumor suppression associated with Maspin
protein. In order to determine if the Maspin protein expression
is important in carcinogenesis at other sites, 10 adenocarcinoma and 11
squamous cell carcinomas cell lines were tested for the
Maspin protein expression by Western analysis. Adenocarcinoma cell
lines included 7 ovarian and three endometrial tumor lines, and
squamous cell tumors included 8 cervical carcinoma and 3
oral or skin carcinoma lines. None of the ovarian tumor lines
(0/7) and only one of three of endometrial tumor lines had even moderate
Maspin protein expression. However, seven of eight cervical
carcinoma cell lines and two of three squamous cell carcinoma
cell lines (SCC4 and A431) highly expressed the Maspin protein.
Immunohistochemistry was done on tumor specimens from 27 ovarian and 9
esophageal carcinomas. 44% (12/27) of ovarian tumors and 77% (7/9)
esophageal carcinoma specimens had either focal or diffuses Maspin
immunoreactivity determined by an immunohistochemical staining using a
polyclonal antibody. Our results indicate that the expression of
Maspin plays a role in several human tumors, including ovary,
cervix, endometrium, esophagus and tongue. The Maspin protein
expression was less common in adenocarcinomas but was commonly
overexpressed in squamous cell carcinomas.

L3 ANSWER 2 OF 3
ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

surface .
AUTHOR ( S ) :
Nadine;

1998:42639 BIOSIS

PREV199800042639

Maspin is an intracellular serpin that partitions
into secretory vesicles and is present at the cell

Pemberton, Philip A. (1); Tipton, A. Rene; Pavloff,

Zahi M.

CORPORATE SOURCE:

SOURCE:

DOCUMENT TYPE:
LANGUAGE :
AB

Richmond, CA

(Dec.

Smith, Jason; Erickson, James R. ; Mouchabeck,
Kiefer, Michael C.

(1) LXR Biotechnol. Inc., 1401 Marina Way S. f
94804 USA

Journal of Histochemistry and Cytochemistry,
1997) Vol. 45, No. 12, pp. 1697
-1706.

ISSN: 0022-1554.
Article
English

The tumor suppressor maspin (mammary serpin) was originally
identified as a component of human mammary epithelial cells that is
downregulated as mammary tumor cells progress from the benign to the
invasive and metastatic states. Maspin inhibits cellular
invasion, motility, and proliferation, but its mechanism of action is
currently unknown. Because the cellular machinery responsible for these
processes is cytoplasmic, we have reexamined the tissue distribution and
subcellular localization of maspin- We find that maspin
, or a maspin-like protein, is present in many human organs, in
which it localizes to epithelia. In cultured human mammary myoepithelial
cells, maspin is predominantly a soluble cytoplasmic protein
that associates with secretory vesicles and is present at the cell
surface. In vitro assays show that the vesicle association is due to the
existence of an uncleaved facultative secretion signal that allows small
amounts of maspin to partition into the endoplasmic reticulum.
These results demonstrate that maspin is more widespread than
previously believed. The subcellular localization studies indicate
soluble intracellular and vesicle associated maspin probably
play an important role in controlling the invasion, motility, and
proliferation of cells expressing it, whereas extracellular maspin
may also regulate these processes in adjacent cells.

that

ACCESSION NUMBER:
DOCUMENT NUMBER:
TITLE:

1978:247280 BIOSIS
BA66:59777

DIFFERENCES IN PATHOLOGICAL CHARACTERISTICS AND PROGNOSIS
OF CLINICAL A- 2 PROSTATIC CANCER FROM A-l AND B DISEASE.

AUTHOR ( S )
CORPORATE

SOURCE:

KURUSU S

N . Y. VETERANS ADM.

SOURCE :

FILE SEGMENT:
LANGUAGE :
AB

stages Al to B2
The study compared

with

GOLIMBU M; SCHINELLA R; MORALES P;
DEP. UROL., N.Y. UNIV. MED. CENT . ,
HOSP., NEW YORK, N.Y., USA.
J UROL, (1978) 119 (5), 618-622.
COD EN : JOURAA. ISSN: 0022-5347.
BA; OLD
English

A retrospective study was done of 53 cases of clinical
prostatic carcinomas staged by pelvic lymphadenectomy .
the histologic differentiation, degree of lymphocytic infiltration,
incidence of lymph node metastases and type

of cellular response of clinical stage A2 to stages Al and B disease. The
available data pertaining to the incidence and survival of patients with
stage A2 prostatic carcinoma were analyzed. One of every 3 unsuspected
carcinomas is of clinical stage A2 . The stage A2 tumors are diffused,

a higher degree of undif f erentiation and a higher incidence of
lymph node metastases than tumors

classified as stage Al and Bl . Survival of patients
with clinical stage A2 tumors is lower than

survival of patients with clinical stage Bl disease. Clinical

stage A2 tumors are more advanced biologically than clinical stage Bl

tumors .

Lll ANSWER 4 OF 23
ACCESSION NUMBER:
TITLE (ENGLISH) :
TITLE { FRENCH) :
INVENTOR(S) :

PATENT ASSIGNEE (S) :
LANGUAGE OF PUBL. :
DOCUMENT TYPE:
PATENT INFORMATION:

PCTFULL COPYRIGHT 2003 Univentio
1998011238 PCTFULL ED 20020514
PROTEASE M, A NOVEL SERINE PROTEASE
PROTEASE M, UNE NOUVELLE SERINE PROTEASE
ANISOWICZ, Anthony;
SAGER, Ruth;
SOTIROPOULOU, Georgia
DANA-FARBER CANCER INSTITUTE
English
Patent

NUMBER

KIND

DATE

WO 9811238 A2 19980319

DESIGNATED STATES

W: AU CA JP AT BE CH DE DK ES FI FR GB GR IE IT LU MC NL

PT SE

APPLICATION INFO.: WO 1997-US16175 A 19970911

PRIORITY INFO. : US 1996-60/025,301 19960913

ABEN Isolated nucleic acid molecules encoding a novel serine protease,
Protease M, is disclosed.

Protease M is downregulated in metastatic mammary epithelial tumor
cells, as well as other tumor

cells, and is upregulated in senescent cells. In addition to isolated
nucleic acid molecules, the

invention provides antisense nucleic acid molecules, recombinant
expression vectors containing a

nucleic acid molecule of the invention, host cells into which the
expression vectors have been

introduced and non-human transgenic animals in which a Protease M gene
has been introduced or

disrupted. The invention further provides isolated Protease M proteins,
fusion proteins, antigenic

peptides and anti-Protease M antibodies. Diagnostic assays, drug
screening assays, and therapeutic

methods utilizing compositions of the invention are also provided.
ABFR Molecules nucleotidiques isolees codant une nouvelle serine protease,
la

protease M» Cette

protease est obtenue par regulation negative dans des cellules
metastatiques de tumeurs epitheliales

mamrnaires, ainsi que dans d'autres cellules tumorales, et elle est
obtenue par regulation positive

dans des cellules senescentes. On decrit par ailleurs des molecules
nucleotidiques anti-sens, des

vecteurs d' expression recombines contenant une molecule nucleotidique
visee dans 1 ! invention, des

cellules hotes dans lesquelles les vecteurs d f expression ont ete
introduits, et des animaux

transgeniques non humains dans lesquels on a introduit ou dissocie un
gene de protease M. On decrit

par ailleurs des proteines de protease M isolees, des proteines
fusionnees, des peptides

antigeniques et des anticorps anti-protease M, et par ailleurs, des
dosages diagnostiques , des

methodes de criblage de medicaments ainsi que des precedes
therapeutiques faisant appel aux

compositions specif iees .

DESCRIPTION Protease M RNA 6A2 RNA EXP

EXP

T24 bladder transitional cell - -
carcinoma

A549(CCL 1 85) lung carcinoma - -
Calu- I lung epidermoid carcinoma - -

Oat 4 lung small cell carcinoma - -
G-361 malignant melanoma - -
SMKE 30 malignant melanoma - -
A2058 malignant melanoma - -
SCC-25 tongue squamous cell - -

carcinoma
RD rhadomyosarcoma of pelvis - -
Kaposi kaposis sarcoma - -
FS3 foreskin fibroblast - -
Leukocyte normal leukocytes - -
- 72 -

TABLE 5. SHOWS RNA EXPRESSION IN MAMMARY TISSUE

SAMPLE TYPE Protease MASPIN CX2 6 CX43

8IN N cell strain ++ +++-+- +++

Lll ANSWER 7 OF 23 PCTFULL COPYRIGHT 2003 Univentio
ACCESSION NUMBER: 1995020041 PCTFULL ED 20020514

TITLE (ENGLISH) : IMMORTALIZED HUMAN MYOEPITHELIAL CELLS AND THEIR USES

TITLE (FRENCH) : CELLULES MIOEPITHELIALES HUMAINES IMMORTAL I SEES

INVENTOR (S) : BARSKY, Sanford, H.;

STERNLICHT, Mark

PATENT ASSIGNEE(S): THE REGENTS OF THE UNIVERSITY OF CALIFORNIA

LANGUAGE OF PUBL. : English
DOCUMENT TYPE: Patent
PATENT INFORMATION:

NUMBER KIND DATE

WO 9520041 Al 19950727

DESIGNATED STATES

W: JP AT BE CH DE DK ES FR GB GR IE IT LU MC NL PT SE

APPLICATION INFO.: WO 1995-US858 A 19950120

PRIORITY INFO. ; US 1994-8/184,720 19940121

ABEN Methods and compositions are provided for the culture of human primary
carcinomas and in situ

carcinomas. Feeder layers derived from a human parotid basal cell
carcinoma, having the HMS-1

phenotype, are able to support the growth of the primary carcinomas,

and

allow for spheroid

formation. Invasion inhibiting factors active against human tumors,
derived from HMS-1, are also

provided. Human basement membrane and extracellular matrix is provided,
produced by a tumorigenic

cell line, where the basement membrane and extracellular matrix can be
used for the growth of a

variety of cells, in culture and in vivo. Other related cell lines are
provided, which can serve to

evaluate in vivo the response of tumorigenic cells to various agents,
including basement membrane

and extracellular matrix. The basement membrane and extracellular

matrix

finds use in allowing the

growth of cells in culture and in vivo, particularly cells which are
otherwise refractory to
xenograf ting .

ABFR L 1 invention concerne des procedes et des compositions permettant la
culture de carcinomes

primaires humains et de carcinomes in situ. Des couches nourricieres
derivees d'un carcinome

basocellulaires de parotyde humaine, presentant le phenotype HMS-1,
peuvent soutenir la croissance

des carcinomes primaires, et permettent la formation de spheroides. Des
facteurs inhibant

1' invasion, agissant contre les tumeurs humaines, derives de HMS-1,

sont

egalement decrits .

L 1 invention concerne egalement une membrane basale et une matrice
extracellulaire humaine, produite

par une lignee cellulaire tumorigene, cette membrane basale et cette
matrice extracellulaire pouvant

etre utilisees pour permettre la croissance d'une variete de cellules,
en culture et in vivo.

L' invention concerne egalement d'autres lignees cellulaires qui peuvent
servir pour evaluer in vivo

la reponse de cellules tumorigenes a divers agents, y compris ladite
membrane basale et ladite

matrice extracellulaire . Cette membrane basale et cette matrice
extracellulaire sont utilisees pour

permettre la croissance de cellules en culture et in vivo, en
particulier de cellules qui autrement
sont refractaires a 1 ' heterogref f e .

Maspin mRNA expression was determined by northern blot
analysis using a I

kb maspin cDNA probe. The expression of TIMP- 1 was also
determined, using the

0.7 kb cDNA insert of pEPA. Poly-A selected rnRNA. . . gel,
transferred to nylon membrane and hybridized with

32p-labeled probe. Protease inhibitor expression was examined for rnRNA
isolated

from HMS-1, salivary gland epidermoid carcinoma

cells (A253; ATCC HTB 41),

normal human prostate derived fibroblasts (NHF) , MDA-MB-231 breast
adenocarcinoma cells (ATCC HTB 26), and a human diploid.

DOCUMENT NUMBER: 126:221310

TITLE: mMaspin: The mouse homolpg of a human tumor

suppressor

gene inhibits mammary tumor invasion and motility
AUTHOR(S) : Zhang, Ming; Sheng, Shijie; Maass, Nicolai; Sager,

Ruth

CORPORATE SOURCE: Dana Farber Cancer Institute, Harvard Medical School,

Boston, MA, 02115, USA
SOURCE: Molecular Medicine (New York) (1997), 3(1), 49-59

CODEN: MOMEF3; ISSN: 1076-1551
PUBLISHER: Springer
DOCUMENT TYPE: Journal
LANGUAGE: English

AB The human maspin gene encodes a protein in the serine proteinase

inhibitor (serpin) family with tumor-suppressing functions in cell
culture

and in nude mice. In order to examine the role of maspin in an

intact mammal, we cloned and sequenced the cDNA of mouse maspin.

The recombinant protein was produced and its activity in cell culture was

assessed. Mouse maspin (mMaspin) was cloned by screening a

mouse mammary gland cDNA library with the human maspin cDNA

probe. Northern blot anal, was used to examine the expression patterns

mouse tissues, mammary epithelial cells, and carcinomas. Recombinant
mMaspin protein was produced in E. coli. Invasion and motility assays
were used to assess the biol. function of mMaspin. MMaspin is 89%
homologous with human maspin at the amino acid level. Like its
human homolog, mMaspin is expressed in normal mouse mammary epithelial
cells and down-regulated in mouse breast tumor cell lines . The
expression

is altered at different developmental stages in mammary gland. Addn. of
the recombinant mMaspin protein to mouse tumor cells was shown to inhibit
invasion in a dose-dependent manner. As with the human protein,
recombinant mMaspin protein also inhibited mouse mammary tumor motility.
Deletion in the putative mMaspin reactive site loop (RSL) region resulted
in the loss of its inhibitory functions. MMaspin is the mouse homolog of
a human tumor suppressor gene. The expression of mMaspin is
down-regulated in tumor cells and is altered at different developmental
stages of mammary gland. MMaspin has inhibitory properties similar to
those of human maspin in cell culture, suggesting that the
homologous proteins play similar physiol. roles in vivo.

Cancer Res. 1981 May;4 1(5): 1657-63.
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